The sporadic occurrence of paroxysmal tachycardias has been a substantial obstacle to developing an objective and quantitative description of their clinical course and to understanding the mechanisms for their successful therapy. The purpose of this study is to develop an objective and quantitative description of three paroxysmal tachycardias (paroxysmal atrial tachycardia, paroxysmal atrial fibrillation, and paroxysmal atrial flutter) treated by drugs from three different classes: a slow response blocker (diltiazem), a beta adrenergic blocker (atenolol), and a primary antiarrhythmic with physiologic properties resembling type I antiarrhythmic drugs (pirmenol). Patients with these arrhythmias will be admitted to the Clinical Research Unit of Duke University Hospital to initiate drug therapy, to measure pharmacokinetics, and to measure pharmacodynamics (PR interval prolongation, QTc interval prolongation, and resting bradycardia for patients taking diltiazem, pirmenol and atenolol, respectively) before beginning outpatient therapy. Recurrence of arrhythmias will be documented using telephone transmission of the electrocardiogram. The elapsed time from the start of therapy to the first recurrence of tachycardia (tachycardia-free interval) will be measured precisely in days. Patients with recurrent arrhythmias will have the dose of their drug increased. Efficacy of each drug will be established using a randomized, double-blind, placebo-controlled cross-over trial. The tachycardia-free intervals measured for each drug regimen will be combined using the Kaplan-Meier life table method as an objective and quantitative statistical description. The Cox proportional hazard model then will be used to test whether plasma drug level or acute pharmacodynamic effects are predictors of drug efficacy. In addition, the pharmacodynamics of diltiazem will be explored to test the hypothesis that bolus diltiazem is more potent than oral administration or loading and maintenance infusion to achieve steady state drug levels, analogus to the variable potency of verapamil. Finally, we will prove that cimetidine, which is not an antiarrhythmic, potentiates the negative dromotropic effect of verapamil (measured as PR interval prolongation) by comparing verapamil + placebo to verapamil + cimetidine in a double-blind fashion.